Sheep Health & Production

Introduction | Yersiniosis | Coccidiosis | Campylobacteriosis | Differential diagnosis of scouring in weaners | Eperythrozoon ovis | Other disease conditions of weaner sheep | Recommended reading

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Introduction

There is an inter-relationship between nutrition, management and pathogenic organisms in a number of clinical disease syndromes in sheep and this is particularly evident in weaner sheep.

Nutrition - energy, protein, trace elements and macro-elements

• as pasture plants flower and senesce, their digestibility falls dramatically and with it the energy value of each kilogram of pasture dry matter
• weaner sheep over 8 to 10 weeks of age are capable of consuming at least as much dietary organic matter as mature sheep per unit of metabolic liveweight (W^0.75), with similar changes in liveweight[1]
• at 20 kg liveweight, weaner Merino sheep have only approximately 1 kg of fat but fat reserves increase rapidly with increased liveweight[2]Dietary energy deficiencies in lambs under 20 kg will result in the mobilization of body protein stores for energy production, with consequent deleterious effects on strength and resilience of the animal
• failure to provide sufficient energy (and protein) for low liveweight weaners leads to weakness, death from malnutrition and susceptibility to intercurrent disease
• consequently, weaners are often the first group on the farm to require supplementation at the end of the growing season as pasture feed deteriorates in quality (as discussed in Chapter 6)
• if the dietary supply of trace elements is low, young sheep are often the first, or only, group of sheep on the farm to exhibit signs of deficiency because of their high requirements for growth and limited opportunities to build up reserve stores

Management

• ewe flock management affects the size and health of lambs at weaning - selection of lambing time, duration of lambing period, ewe nutrition before and during lactation, parasitism of ewes and lambs before weaning all have consequences for the size and health of weaners in the subsequent months
• lamb management at weaning - the benefits of weaning 13 weeks after the start of lambing are, for the lambs, removal from parasite-contaminated pastures and, for the ewes, the cessation of lactation and increased production of wool; the disadvantages include increased stress on lambs, particularly if it is still winter or early spring, and an increased risk of intercurrent disease. The occurrence of diarrhoea, even in the absence of disease processes, may also be considered a disadvantage of weaning lambs at that age

Intercurrent diseases

At the time of weaning, lambs are young, recently mulesed, distressed about their maternal separation, still learning to graze effectively and, in late winter at least, often wet and cold and grazing short pastures with very high water content. By virtue of these stressors, their immunological inexperience and other predisposing factors, weaners may have a high prevalence of helminthosis, fleece-rot, dermatophilosis and fly strike, contagious pustular dermatitis, pneumonia and arthritis unless effective preventive measures are taken.

In addition, there are three or four diseases which are almost exclusively seen in weaners and which relate to the environmental and nutritional conditions under which they are managed. These diseases are yersiniosis, coccidiosis, eperythrozoonosis and, possibly, campylobacteriosis and they will be discussed in detail in the following pages. Successful management and health maintenance programs for weaners will reduce the incidence of these diseases and, if they do still occur, reduce their impact on the flock.

Preventive medicine program for Merino weaners

The requirements of a preventive medicine, or health maintenance, program for Merino weaners in the medium and high rainfall districts of Australia can be divided into 5 interrelated steps.

1. Plan for an uninterrupted weight gain from birth to a reasonably robust size; 22kg for fine wool Merinos, 26kg for medium wools, 30kg for strong wools. Under most Australian conditions in which Merinos are raised, there is at least one period in their first year of life when weaners are likely to lose weight for a period of weeks or months, unless special steps are taken to prevent weight loss. It is during this period of weight loss that the young sheep are at greatest risk. Their ability to withstand the effects of intercurrent diseases and nutritional deprivation is enhanced if they have achieved these liveweights. Planning involves consideration of the time of lambing, nutritional management of the ewe flock and the expected seasonal variation in feed availability on the farm in question
2. Establish reliable practices to prevent or control diseases for which the cost-benefit clearly favours preventive action every year. Helminthiasis and trace element deficiencies are two notable examples of this group
3. Introduce monitoring programs and 'action triggers' for preventive programs for other diseases which occur from time to time. Fly strike or grass seed infestations may fall into this category. Monitoring programs may be as simple as a 'reminder' system; 'action triggers' for fly strike prevention may include 'rainfall after November' or the presence of fly activity detected in twice weekly inspections
4. Attend to the 'tail' of the mob. 10% to 20% of the mob of weaners will be significantly lighter or weaker than the rest and will probably experience the highest mortality from any disease processes which affect the mob. Identification of this sub-group for special attention may reduce the expense of preventive action and improve the economic efficiency of preventive programs
5. Plan the timing and level of supplementary feeding in advance. Have access to sufficient suitable supplements and introduce them before health or production problems emerge

Yersiniosis

Yersiniosis is an enterocolitis, with mesenteric lymphadenitis, caused by infection with Yersinia pseudotuberculosis or, possibly, Y enterocolitica. Clinically, the disease is marked by persistent diarrhoea with a low to moderate prevalence, low mortality and a noticeable failure to thrive of affected animals. It occurs most commonly in animals 3 months to 18 months of age. Microabscessation in the lamina propria of the distal half of the small intestine is a characteristic histological finding.

Both Yersinia pseudotuberculosis[3] and Y enterocolitica can be isolated from apparently normal sheep.Y pseudotuberculosis is the species more frequently isolated from field cases. Serotype III is more commonly isolated from sheep cases than types I and II. Experimentally, the disease has been reproduced both in terms of infection with microabscessation in the intestinal mucosa and clinical disease with this species of the bacterium.

Yersinia enterocolitica, mainly biotype 5, serotype 02,3, has also been isolated from affected sheep in Australia. The infection, with microabscesses, has been reproduced experimentally with this species but clinical disease has not. The pathogenicity of this organism for sheep remains unclear[4].

Epidemiology

The disease is usually seen in late winter and spring in winter rainfall areas or at all times of the year in other regions. The onset of cold, wet windy weather, particularly if associated with stressful events like weaning or shearing, appears to be an important predisposing factor. The events which lead to the development of the disease are poorly understood.The organism is present in apparently healthy sheep so possibly, under conditions of stress, carrier animals commence or increase the excretion of the organism, providing the potential to infect susceptible sheep. As well as sheep, gregarious birds and rodents may serve as carriers of the organism and can be responsible for its spread.Infection is by the oral route. Disease may in part be due to the compromise of cell mediated immunity, permitting establishment of invading organisms or the recrudescence of latent infection[5].

Pathogenesis

Pathogenic strains of Yersinia spp have the capacity, conferred by surface proteins, to attach to and invade epithelial cells lining the gut and to resist phagocytosis and other host attempts to kill the bacteria. The bacteria attain the lamina propria, where they form microcolonies and host inflammatory responses produce microabscesses.An enterotoxin which causes hypersecretion enhances virulence but is not essential for the development of the disease.

Clinical findings

Clinically, there is a dark green to black diarrhoea, which tends to be mild and chronic and which leads to dagginess on the perineum and hocks. Tenesmus may be present. Affected sheep are mildly dehydrated, in poorer condition than expected from available feed, and the mortality rate is generally lower than 2%. The true mortality rate due to yersiniosis is difficult to ascertain accurately because of the (usual) presence of intercurrent disease, particularly nematodiasis.

Necropsy findings

Gross lesions are minimal.Intestinal contents are abnormally fluid and the wall of the small intestine, caecum and colon may show some thickening, congestion and oedema. Small foci of pallor, haemorrhage and erosions less than 0.5cm in diameter may be evident. Mesenteric lymph nodes are congested and oedematous. If the liver is involved there may be a multifocal, necrotizing hepatitis. Histopathology reveals an acute segmental erosive enteritis with microabscesses, more prevalent in the jejunum and ileum than in the large intestine.

Diagnosis

Nematodiasis should be ruled out by history, faecal egg count, and total worm count if necessary. Definitive determination of the nature of the bacterial infection in the live animal is difficult. After necropsy, bacteriology on liver, spleen, mesenteric lymph nodes and intestinal contents of the jejunum, ileum, caecum and colon, using selective media will confirm the diagnosis. Some fixed sections of gut should also be taken for histopathology (refer to Diseases of the Alimentary System for details of sample collection).

Treatment and prevention

Tetracyclines should be effective but treatment is often of uncertain usefulness due to the persistent predisposition in most cases and the serial nature of infection through a mob of sheep. Steps should be taken to improve the environmental conditions for the sheep - reducing exposure, improving nutrition and attempting to reduce the stress associated with management practices as much as possible, particularly for young sheep. Probably a major improvement can be obtained if the periods that young sheep are yarded off feed are kept as few and as short as possible.Internal parasite control is also important in reducing the susceptibility to yersiniosis.

Coccidiosis

Coccidiosis is most common in lambs 2 to 6 months of age run under crowded conditions, such as feedlots or at high densities on pastures. The disease is not common in Australia, but only because lambs are not often managed under such conditions. When they are, however, there is a significant risk of coccidiosis.

Aetiology

The disease in sheep is caused by a number of Eimeria spp (Table 12.1). Mixed infections, by virtue of a wider distribution of infection in the gut, are often more severe than infections restricted to one or few species, and mixed infections are the general rule.

Table 12.1 Eimeria spp infecting sheep in Australia

Pathogenesis

The pathogenesis of coccidiosis is related to the massive amplification of infection which occurs within the cells of the intestinal mucosa of each susceptible host and the cellular damage caused by the developing stages. Each ingested oocyst gives rise to 8 sporozoites and each of these enters a mucosal cell. One or more cycles of asexual division, termed merogony, follow, releasing many merozoites (hundreds or thousands from each sporozoite, depending on the species) each of which in turn invades a cell and either continues another cycle of asexual multiplication or diverts into the sexual phase and forms a gamont. After fertilization, oocysts are produced within mucosal cells then released and passed in the faeces.

The damage done to the infected cell varies with the infecting species and varies from functional disturbance to the loss of surface epithelial cells and villus atrophy. Acute inflammatory reactions are most commonly associated with destruction of cells by the sexual stages and oocysts rather than a response to asexual stages. The Eimeria spp which are the most pathogenic in sheep are those which invade the ileum, caecum and colon, rather than those in the jejunum. Virulence is also a function of the biotic potential of the parasite (the degree of asexual replication) and the degree of host response to infection. In any one episode of exposure to coccidia, the severity of signs also depend on the size of the infecting dose and the susceptibility of the host. The untoward effects of infection mainly relate to malabsorption induced by villus atrophy, hypoproteinaemia and dehydration due to exudative enteritis and colitis caused by epithelial erosion and ulceration.

Epidemiology

Coccidia are normally present in healthy sheep of all ages and small numbers of oocysts are usually present in the faeces. Disease outbreaks occur when susceptible animals are exposed to pasture infection, left on the same pasture for long enough to amplify the infection significantly and exposed to the greatly increased levels of infectivity in a time too short for a useful degree of immunity to develop. This process is much more likely to occur when stocking rates are very high.

The pre-patent period of most ovine coccidia is 16 to 20 days. Typically, then, outbreaks of coccidiosis occur 2 to 3 weeks after young animals are confined on suitable pastures and oocyst output peaks 4 to 5 weeks after confinement, remains high for 1 to 3 weeks, then declines.

The primary source of infection is usually the lambs or weaners themselves. Oocysts can survive prolonged periods on pasture provided humidity is high.They do not survive prolonged dry periods or cold periods. Small amounts of contamination may survive from one season to the next, but the most significant source of infection is generally contemporaneous.

Infection does not persist in the host without constant reinfection. Consequently, moving animals away from heavily contaminated paddocks to 'clean' pastures at normal stocking rates will prevent the development of new cases after a week or two and allow chronic cases to recover.

The effect of host immunity appears to be a dramatic reduction of the biotic potential of the coccidia. Thus adult sheep may remain constantly exposed and constantly infected at low levels, providing a low level of contamination for young sheep.

Clinical signs

In acute coccidiosis diarrhoea is the predominant sign (but not usually dysentery which occurs more commonly in calves), with depression, anorexia and abdominal pain. Diarrhoea may persist for only three days, by which time the animal has lost significant bodyweight which is slow to return, or the infection may become chronic in some cases.Diarrhoea, weakness and weight loss are the predominant signs in chronic coccidiosis.The faeces is often grey in colour. Mortality rates can be high in some cases.

Necropsy findings

Lesions are most obvious in the terminal ileum, caecum and proximal colon, and include oedematous thickening of the wall, congestion and haemorrhage and sometimes ulceration in the mucosa. White polyps on the mucosa of the small intestine (0.3 to 1.5 cm in diameter) are a useful diagnostic finding but are generally only associated with infection with E ovina[6].

Diagnosis

The rapid and reasonably synchronous onset of diarrhoea in a number of young sheep within a few weeks of confinement is strongly suggestive of coccidiosis. Nematodiasis should also be considered but can often be ruled out quickly on history or faecal egg count. Faecal oocyst counts can become very high in infected animals; 5,000 to 10,000 oocysts per gram of faeces is not unusual and counts 10 to 100 times as high do occur. High counts, however, do not necessarily indicate disease nor do low counts necessarily mean that coccidia are not causing disease. A definite diagnosis should only be made when the history and clinical signs suggest coccidiosis and those findings are supported by either high oocyst counts or necropsy examination, or both.

Treatment

Sodium sulfadimidine at the rate of 1g per 7kg liveweight per os, preferably daily for 3 days, is recommended (15ml of a 33.3% solution to a 25kg sheep). The disease is, however, self-limiting and most therapies are ineffective against the late stages of the parasite.

Control

Prevention rests on avoidance of overcrowded conditions, particularly when the weather is warm and ground conditions are moist.If these conditions cannot be avoided, continuous medication can be attempted. Amprolium (500mg/kg of feed), monensin (2mg/kg liveweight or 20mg/kg of feed) and lasalocid (25-100mg/kg of feed) can be used for preventive treatment.Amprolium, however, is a thiamin inhibitor and care must be taken to avoid the occurrence of PEM. Monensin reduces weight gain[7].

Campylobacteriosis

Campylobacter jejuni has been isolated from sheep and it is possible to produce enteritis experimentally with the organism. A number of other Campylobacter spp have been isolated from the intestinal tracts and faeces of both healthy and diseased sheep-including C faecalis, C coli, C fetus subsp fetus. Campylobacter spp bacteria are difficult to isolate, a problem which has added to the difficulty of experimental reproduction of Camplylobacter enteritis. In Victoria, a clinical syndrome called weaner colitis has been associated with Campylobacter-like organisms[8][9][10], but firm proof of the aetiology of this disease is lacking.

Differential diagnosis of scouring in weaners

As well as yersiniosis, enteritis and diarrhoea are also commonly seen in weaners due to nematodiasis, coccidiosis, grain poisoning and salmonellosis. Diarrhoea is a minor clinical finding in enterotoxaemia, poisoning with copper, organophosphates, phosphorus, selenium and several plant intoxications.[11]

Eperythrozoon ovis

Eperythozoonosis is characteristically a disease of weaner sheep but in fact sheep of all ages are susceptible. Mature sheep with no previous experience of infection are as badly affected as weaners[12]. Merino sheep are particularly susceptible.Epizootics occur when 3 particular conditions come together - susceptible animals, a source of infection and a vector. Recovered animals remain infected for long periods, probably for life, and are premune[13]. The flock prevalence in southern Australia is very high: at least 90%[14].

Transmission and infection

The incubation period in cases of natural infection is 1 to 6 weeks.Transmission occurs by flying insects, such as mosquitoes. There is no transplacental or intra-uterine transmission. Episodes of infection last 14 to 28 days.These episodes are sometimes followed by a series of cycles at intervals of 2 to 4 months. The Coombs test is positive from the time that parasitaemia is maximal until up to 6 months after the parasites are no longer detectable.

Clinical and necropsy signs

Sheep infected with E ovis are anaemic, which leads to weakness and a reduction in exercise tolerance. Slight to moderate icterus is sometimes observable, particularly 3 to 4 days after stress has exacerbated an already existing infection.E ovis is probably a frequent contributor to the development of the 'tail' that occurs often in a moving mob of weaner sheep. Although not observable clinically, infection may also reduce wool production, by 5% to 10% in the year of first infection, and bodyweight gain over the period of infection[15].

At necopsy, splenomegaly is a prominent feature and the haemal nodes are enlarged.

Laboratory aids to diagnosis

A blood profile reveals anaemia, often severe, with a macrocytic, hypo- or normochromic regenerative response.Parasites may appear in smears but often they disappear about the same time as anaemia develops. The Coombs (anti-globulin) test is not specific for E ovis but, because other causes of a positive test are unusual, is a useful diagnostic aid. A CFT[16][17].

Treatment and control

Infection and spread of E ovis is inevitable if the vector and infected sheep are present. In attempting to control the disease, weaners should be maintained in good nutritional state and free from intercurrent diseases. Tetracycline and oxytetracycline are effective therapies for E suis infection in pigs so are rational treatments for sheep.

Other disease conditions of weaner sheep

There are a number of other disease conditions which affect weaner sheep and some of these can add to the variety of conditions which often affect flocks of Merino weaners simultaneously. It is not unusual to find most of these conditions present in one mob of Merino weaner sheep. All of these conditions are discussed in other sections of the notes. They include :-

Fleece-rot and fly strike       Dermatophilosis

Vitamin & trace element deficiencies       Helminthosis

Contagious pustular dermatitis       Arthritis

Pneumonia

Recommended reading

Allworth MB (1990) Weaner illthrift - treatment and prevention In Sheep Medicine , University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 141, p 435

Collins GH (1992) Veterinary parasitology Notes for veterinary undergraduates, Department of Veterinary Pathology, University of Sydney, section 7.31

Glastonbury JRW (1990) Non-parasitic scours in sheep In Sheep Medicine, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 141, p 459

Wilkinson FC (1981) Lamb survival from marking and weaner illthrift In Refresher Course on Sheep, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 58, p 193

[1] Egan JK and Doyle PT (1982) The effect of stage of maturity in sheep upon intake and digestion of roughage diets Aust J Agric Res 33 p 1099

[2] Allden WG (1970) The body composition and herbage utilization of grazing Merino and crossbred lambs during periods of growth and summer undernutrition Aust J Agric Res 21 p 261

[3] Slee KJ and Button C (1990) Enteritis in sheep, goats and pigs due to Yersinia pseudotuberculosis infection Aust Vet J 67 p 320

[4] Slee KJ and Button C (1990) Enteritis in sheep and goats due to Yersinia enterocolitica infection Aust Vet J 67 p 396

[5] Barker IK, van Dreumel AA and Palmer N (1993) The alimentary system In Pathology of Domestic Animals, 4th ed, KVF Jubb, PC Kennedy and N Palmer (eds) Academic Press

[6] Glastonbury JRW (1990) Non-parasitic scours in sheep In Sheep Medicine, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 141, p 459

[7] Munday BL (1981) Coccidiosis (including Globidiosis) In Refresher Course on Sheep, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 58, p 27

[8] Stephens LR (1983) Weaner colitis in sheep due to Campylobacter-like bacteria In Sheep Production and Preventive Medicine, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 67, p 53

[9] Stephens LR, Browning JW, Slee KJ, Hayes J and Tzipori S (1984) Colitis in sheep due to a Campylobacter-like bacterium Aust Vet J 67 p 320

[10] McOrist S, Stephens LR and Skilbeck N (1987) Experimental reproduction of ovine weaner colitis with a Campylobacter-like organism Aust Vet J 64 p 29

[11] For a more complete discussion of the differential diagnosis of scouring, consult Chapter 16, Diseases of the Alimentary System.

[12] Sheriff D (1976) Infections with Eperythrozoa and Haemobartonellae In University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 27, p 5

[13] Sutton RH (1990) Eperythrozoonosis In Sheep Medicine, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 141, p 133

[14] Nicholls TJ and Veale PI (1986) The prevalence of Eperythrozoon ovis infection in weaner and adult sheep in north eastern Victoria Aust Vet J 63 p 118

[15] Daddow KN (1979) Eperythrozoon ovis - a cause of anaemia, reduced production and decreased exercise tolerance in sheep Aust Vet J p 433

[16] Daddow KN (1977) A complement fixation test for the detection of Eperythrozoon infection in sheep Aust Vet J 53 p 139

[17] Nicholls TJ and Veale PI (1986) A modified indirect immunofluorescent assay for the detection of antibody to Eperythrozoon ovis in sheepAust Vet J 63 p 157